APPROACH OF

COMATOSE PATIENT

Ken wirastuti
 Introduction
Many patients present to emergency departments
with an altered state of consciousness (3 5%)

The state of coma is marked by a lack of awareness

and response to external stimuli; patients cannot be
roused.

Large proportion of comatose patient recover

Untreated coma may lead to further brain damage

 Introduction
Coma is a medical emergency and may constitute a
diagnostic and therapeutic challenge for the intensivist.

Coma and other states of impaired consciousness

represent a severe derangement in cerebral function
that may be structural or non structural in origin.

Many of the underlying processes leading to coma can

be both life threatening and potentially reversible with
the timely institution of medical or surgical therapy.
 Coma
Coma= state of deep sleep
Coma is a profound state of unconciuosness
A person in a coma can not be awakened
Fails to respond normally to pain, light or sound
Does not have sleep-wake cycle
Does not take voluntary actions
A person in a state of coma can be described as
comatose
 Coma is a state in which patient is
unarousable and unresponsive and any
response to repeated stimuli is only primitive
avoidance reflex.
 Etiologi of Coma
Intracranial Extracranial
Metabolik
Infections Diabetic coma
hypoglicemia
Mass lesion Hepatic encephalopathy
Uremic encephalopathy
Trauma Alkalosis/acidosis
Electroliyte
Vascular Hyper/hyponatremia
Hypercalsemia
Respiratory
Hypoxia
Hypercarbia
Drugs, toxins
 Classification
From a pathophysiologic standpoint, coma
may be viewed as the expression of

a) Primary insults to the cerebral cortex,

diencephalic structures, midbrain or rostral
pons; and
b) Secondary cerebral manifestations of
systemic toxic, metabolic or endocrine
derangements.
 Classifications

Supratentorial lesions cause coma by either

widespread bilateral disease, increased intracranial
pressure, or herniation.
Infratentorial lesions involve the RAS, usually with
associated brainstem signs
Metabolic coma causes diffuse hemispheric
involvement and depression of RAS, usually without focal
findings
Psychogenic
Plum and Posner, 1982
 To affect consciousness,
lesions of the cerebral cortex
must involve both
hemispheres or must be
unilateral lesions large enough
to cause displacement of
midline structures

Brainstem and diencephalic

lesions resulting in coma may
be comparatively small;
however they may also involve
bilateral structures.
 Supratentorial Mass Lesions
Pathophysiology

Altered consciousness is based on

Increased intracranial pressure
Herniation
Diffuse bilateral lesions
Infratentorial Lesions
INFRATENTORIAL

Cause coma by affecting reticular

activating system in pons
Brainstem nuclei and tracts usually
involved with resultant focal brainstem
findings
 Physiology
Cerebral neurons are fully dependent on cerebral blood flow
(CBF) and the related delivery of oxygen and glucose. CBF is
~75 mL per 100 g/min in gray matter and 30 mL per 100
g/min in white matter (mean = 55 mL per 100 g/min); oxygen
consumption is 3.5 mL per 100 g/min, and glucose utilization
is 5 mg per 100 g/min.

Brain stores of glucose provide energy for ~2 min after blood

flow is interrupted, and oxygen stores last 810 s after the
cessation of blood flow.
Simultaneous hypoxia and ischemia exhaust glucose more
rapidly.
 The Comatose Patient
Neurophysiology
Wakefulness depends on the integrity of
both cerebral hemispheres and the
ascending reticular activating formation of
the brain stem.
Consciousness requires:
An intact pontine reticular activating system
An intact cerebral hemisphere, or at least
part of a hemisphere
Coma requires dysfunction of either the:
Pontine reticular activating system, or
Bihemispheric cerebral dysfunction
 Coma Pathophysiology

Bilateral cerebral cortex dysfunction

Toxic/metabolic
Mass lesion, Increased ICP
Cerebral ischemia/hypoperfusion, Infarct

Brainstem suppresion of reticular activating

system (RAS)
Ischemia, Infarct
 Approach
ABC
Immediate management
Maintain iv line, oxygen inhalation, blood sample,
control seizure, consider iv glucose, thiamine,
naloxon
Examination
History
Investigations
 Airway

Evaluate -- is airway patent. Can patient move air without

obstruction. Is there trauma or foreign body obstructing
airway
Place airway if indicated - nasal or oral airway, intubation,
or surgical airway
Intubate (protecting neck) anyone who will let you
Any of the following are adequate criteria
GCS < 9
Airway not secure or open
Respiration not adequate
Any significant respiratory failure
Uncertainty regarding direction or rate of mental status changes,
particularly if constant observation not available (during CT scans,
etc..)
 Breathing
Evaluate - is patient moving adequate air, is
respiratory rate appropriate, is gas exchange
adequate, are breath sounds adequate and
symmetrical
Must assure oxygenation and ventilation
If intubated dont forget to ventilate
Identify and immediately treat problems -
pneumothorax, airway obstruction, etc..
Management of the Comatose Patient
Circulation Circulation
Is patient in shock?
Check pulses, heart rate, blood pressure,
perfusion
Remember hypotension is late sign of shock
Start treatment for shock
Do not restrict fluids in comatose patient with
inadequate intravascular volume.
Cardiac output and cerebral perfusion are much
more important than fluid restriction
NEUROLOGY EXAMINATION
 Level of Coma
Glasgow Conciousness
Scale (GCS)
Eye opening Best Motor Response
4 - spontaneous 6 - obeys
3 - to speech 5 - localizes
2 - to pain 4 - withdraws
1 - none 3 - abnormal flexion
Verbal Response 2 - abnormal
5 - oriented extension
4 - confused conversation 1 - none
3 - inappropriate words
2 - incomprehensible sounds
1 - none
FOUR Score
 NECK
NUCHAL RIGIDITY: SAH, Encephalitis
Meningeal sign: Meningitis
Reflex Physiology
Reflex Pathology
N. Cranialis
 Assessment of Brainstem Function

Pupillary response
Corneal reflex
Gag reflex
Cough reflex
Oculocephalic reflex (Dolls eyes assessment)
 Pupillary size and reaction
Medium to dilated symmetrical pupils fixed to light structural
disease of the brain stem.
Small symmetrical pupils reactive to light
metabolic diseases and drug overdose.
Unequal pupil fixed to light
intracranial mass lesion producing 3rd nerve palsy e.g in
unilateral uncal herniation.
 Eye movements
Vestibulo-ocular reflexes
Oculo-cephalic reflexes (Doll's eye movement )
Normal response consist of deviation of both eyes
to the opposite direction of head rotation. Again
absence or abnormal response indicates brain-stem
dysfunction.
 Motor Responses- Posturing
Decerebrate rigidityThis refers to bilateral upper and lower
limb extensor posture, usually the consequence of bilateral
mid-brain or pontine lesions.
Decorticate postureThis refers to bilateral flexion of the
upper limbs and extension of the lower limbs, usually the
consequence of an upper brain stem lesion.
Unilateral decerebrate or decorticate postures can be seen
and are an indication of a unilateral lesion.
 Respiratory pattern
(a ) Hyperventilation - midbrain and upper pons lesion
metabolic diseases e.g. hepatic coma, diabetes and generalised
raised intracranial pressure in its early stages.

( b ) Hypoventilation - medullary, upper cervical spinal lesion

Drug overdose and later stages of cerebral herniation.

( e ) Cheyne-Stoke respiration usually diencephalic lesion

central transtentorial herniation and obstructive
hydrocephalus.

( d ) Ataxic respiration (completely irregular breathing)

brain-stem dysfunction of a diffuse nature
a) Cheynes stokes
respiration

b) Central neurogenic
hyperventilation

c) Apneustic breathing

a) Cluster breathing

b) Ataxic / Biots
breathing
ICP elastance curve (change in pressure per unit change in volume)

Stage 1/2 = compensation phase.

Stage 3/4 = decompensated phase.

 RAISED INTRACRANIAL
PRESSURE

ICP

DAYS WEEKS HOURS DEATH

CONING
FOCAL VENTRICULAR HYDROCEPHALUS
DISPLACEMENTS DISTORTION CENTRAL HERNIA
 Clinical Signs of Increased ICP
History of headache, vomiting, severe hypertension,
unexplained bradycadia
Funduscopy: Oedema pupil N.II
CT evidense of elevated ICP
Loss of image of third ventricle
Loss of image of perimesencephalic cistern
In unilateral lesion :
1. Midline shift ( should be visualized at level of Foremen Monro)
2. Dilatation of contralateral ventricles
Physical Changes With Increased Intracranial
Pressure
 Decrease in Ischemic
Perfusion Pressure Brain

High ICP Compression, Distortion,

and Herniation

Death
and
Non-surgical management Disability

Surgical management
 Diffuse Axonal Injury (DAI)
(clinical entity: Diffuse Brain Injury)
Among patients with severe HI, only 50% related to presence of focal
hematomas ( EDH, SDH, ICH/contusion )

Patient with obvious neurologic deficit or loss of

consciousness without significant lesion on CT scan
Radiology: presence of hemorrhagic lesion without
mass effect (tissue tear or petechial hemorrhage), in
subcortical white matter, corpus callosum, basal
ganglia, or brainstem
Other features: diffuse edema, t-SAH, and IVH
 Laboratorium Evaluation
Complete blood count, MP, B.sugar
Blood urea, s. creatinine, s.electrolyte
Blood gases, ALT, AST
CSF examination

Imaging Evaluation
CT Scan / MRI
Rontgen Thorax
EEG
TCD
 Cerebral Circulation

Factors determining cerebral oxygenation

Cerebral Blood Flow (CBF)
Arterial Oxygen Content (CaO2)
Cerebral Metabolic Rate of Oxygen
Consumption (CMRO2)
Autoregulation of cerebral blood flow

CPP = MAP - ICP

Cerebral Blood Flow

CBF = CPP/CVR
MANAGEMENT
Avoid hypotension and hypoxia

Hypoxia (PaO2 < 60 mmHg) and hypotension (SBP <

90 mmHg) are strongly associated with significant
increases mortality (hypoxia: odds ratio [OR] 21,
DO2 cerebral= CBF x CaO2
95% CI 1726; hypotension: OR 27, 95% CI 21
34) CBF = CPP/CVR
Hypertension: SBP > 160 mm Hg or MAP > 110 mm
Hg, can aggravate vasogenic brain edema and
intracranial hypertension
Early restoration CBF may reduce cerebral oedema
in 1st 24 hrs
Circulatory Support:
Maintain Cerebral Perfusion Pressure
CPP = MAP ICP (or CVP)

Manajemen Hipotensi dan hipoksia

Target:
SBP > 90 mmHg
PaO2 > 60 mmHg
CPP > 70 mmHg or MAP > 90 mmHg
Praktek
Resusitasi Cairan
 Correction of anemia: targeted hemoglobin
10 g/L or hematocrit 30
o Increased cerebral DO2 = CBF x CaO2
CaO2 = Hb x 1,34 x SaO2 + PaO2 x 0,003

Vasopressor:
o Norepinephrin. (Dopamine causes
cerebral vasodilatation and increase
ICP)
Management of High ICP
 Decrease ICP : Promote Venous Drainage
Keep neck mid-line and elevate head of bed . To what degree?

CSF
Feldman et al. (1992)
Fluid Journal of
Neurosurgery, 76

March et al. (1990)

Journal of
Neuroscience Nursing,
22(6)

Parsons & Wilson

(1984) Nursing
Research, 33(2)

Image from: Dicarlo in ALL-NET Pediatric Critical Care Textbook

www.med.ub.es/All-Net/english/neuropage/protect/icp-tx-3.htm
 Manitol administration: The effective dose is
0.25-1 g/kg, administered intravenously over a
period of 15 to 20 minutes.

Hypertonic Saline Solution (NaCl 7.5%: 2

mL/kg IV over 15 min)
Decrease Intracranial Pressure:
Management of Pain & Agitation
Problems:
Opiods
Difficult to
Benzodiazepines assess neurologic
exam
Management of Movement Risk of hypoten-
sion Use short
Neuromuscular blockade may be acting agents
required - use only when necessary

Do opiods increase CBF and ICP as well as lower MAP and CPP?
Increased ICP with concurrent decreased MAP and CPP has been
documented with use of opiods. But, elevation in ICP is transient and
there is no resulting ischemia from decreased MAP / CPP.

Albanese et al. (1999) Critical Care Medicine, 27(2)

Decrease Cerebral Metabolic Rate
 Reduction of Cerebral Metabolic Rate

Goal: Reduce cerebral oxygen requirement

Seizure post brain injury (early and late)
Anticonvulsants
Prophylactic use of phenytoin, carbamazepine,
phenobarbital or valproate is not recommended
for preventing late post-traumatic seizures and early
seizure activity
Control of convulsion:
Phenitoin: A loading dose of 15 to 20 mg/kg administered intravenously
(I.V.) over 30 minutes followed by 100 mg, I.V., every 8 hours,
titrated to plasma level, for 7 days,

Traeger et al. (1983) Critical Care Medicine, 11Ward et al. (1985) Journal of Neurosurgery, 62(3)
Reduction of Cerebral Metabolic Rate: Hypothermia

Metz et al. (1996) Journal of Neurosurgery, 85(4)

32.5 C reduced cerebral metabolic rate for oxygen (CMRO2) by
45% without change in CBF
intracranial pressure decreased significantly (p < 0.01)
Marion et al. (1997) New England Journal of Medicine, 336(8)
At 12 months, 62% of patients (GCS of 5-7) cooled to 32-33 C
have good outcomes vs. 38% of patients in control group

Side-effects:
Potassium flux Requires:
No pediatric
Coagulopathy Slow re-warming
Shivering
studies!
Close monitoring
Skin Breakdown
 Conclusion
Coma is caused by a disease process involving bilateral
cerebral hemispheres or a focal lesion affecting brain
stem structures; the initial evaluation should focus on
distinguishing the two
Seizure is a frequently unrecognized cause of stupor
and coma
The prognosis of eventual recovery depends on the
underlying cause
Clinical assessment of coma is useful
It should be as routine as respiratory examination
in respiratory failure